ArticleCellular and molecular life sciences : CMLS2023
Tyrosine kinase SRC-induced YAP1-KLF5 module regulates cancer stemness and metastasis in triple-negative breast cancer.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- Selective antitumor and apoptosis‑inducing effects of the Src inhibitor PP1 in human tongue squamous cell carcinoma cells.International journal of oncology · 2026Article
- An anoikis-related gene signature predicts prognosis and immunotherapy response, and identifies CCAR2 as a therapeutic target in triple-negative breast cancer.Frontiers in immunology · 2026Article
- Honokiol Suppresses Stemness and Sensitizes Triple-Negative Breast Cancer to Chemotherapy via YAP/TAZ-TEAD Inhibition.Oncology research · 2026Article
- Klf5a in Endoderm Promotes Pharyngeal Cartilage Morphogenesis.International journal of molecular sciences · 2025Article
- Decoy Extracellular Vesicles Overcome Triple-Negative Breast Cancer Heterogeneity via Membrane-Cytoplasm-Mitochondria Cascade Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reciprocal regulation of Solo and Src orchestrates Src trafficking to promote mesenchymal cell migration.iScience · 2025Article
- A comprehensive review on targeted therapies for triple negative breast cancer: an evidence-based treatment guideline.Discover oncology · 2025Article
- Porphyromonas gingivalis potentiates stem-like properties of oral squamous cell carcinoma by modulating SCD1-dependent lipid synthesis via NOD1/KLF5 axis.International journal of oral science · 2025Article
- Biguanides antithetically regulate tumor properties by the dose-dependent mitochondrial reprogramming-driven c-Src pathway.Cell reports. Medicine · 2025Article
- N-phenyl pyrazoline derivative inhibits cell aggressiveness and enhances paclitaxel sensitivity of triple negative breast cancer cells.Scientific reports · 2024Article
- TPX2 overexpression promotes sensitivity to dasatinib in breast cancer by activating YAP transcriptional signaling.Molecular oncology · 2024Article
- UCHL1 contributes to insensitivity to endocrine therapy in triple-negative breast cancer by deubiquitinating and stabilizing KLF5.Breast cancer research : BCR · 2024Article
- Breast cancer-derived CAV1 promotes lung metastasis by regulating integrin α6β4 and the recruitment and polarization of tumor-associated neutrophils.International journal of biological sciences · 2024Article
- lncRNA ENST00000422059 promotes cell proliferation and inhibits cell apoptosis in breast cancer by regulating the miR-145-5p/KLF5 axis.Acta biochimica et biophysica Sinica · 2023Article
- Targeting the KLF5-EphA2 axis can restrain cancer stemness and overcome chemoresistance in basal-like breast cancer.International journal of biological sciences · 2023Article
- Decoding the Anti-Tumour Mechanism of ɑ-Solanine: SRC Inhibition and Ferroptosis Induction in Colon Cancer.IET systems biologyArticle
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
SRC is the first identified oncogene, and its aberrant activation has been implicated as a driving event in tumor initiation and progression. However, its role in cancer stemness regulation and the underlying regulatory mechanism are still elusive. Here, we identified a YAP1 tyrosine phosphorylation-dependent YAP1-KLF5 oncogenic module, as the key downstream mediator of SRC kinase regulating cancer stemness and metastasis in triple-negative breast cancer (TNBC). SRC was overexpressed in TNBC patient tissues and its expression level was highly correlated with the tumor malignancy. SRC activation induced, while inhibition of SRC kinase reduced the cancer stemness, tumor cell growth and metastasis in vitro and in vivo. Transcriptomic and proteomic analysis revealed that SRC-mediated YAP1 tyrosine phosphorylation induced its interaction with Kruppel-like factor 5 (KLF5) to form a YAP1/TEAD-KLF5 complex in TNBC cells. YAP1-KLF5 association further promoted TEAD-mediated transcriptional program independently of canonical Hippo kinases, which eventually gave rise to the enhanced cancer stemness and metastasis. Disruption of YAP1-KLF5 module in TNBC cells dramatically attenuated the SRC-induced cancer stemness and metastasis in vitro and in vivo. Accordingly, co-upregulations of SRC and YAP1-KLF5 module in TNBC tissues were significantly positively correlated with the tumor malignance. Altogether, our work presents a novel tyrosine phosphorylation-dependent YAP1-KLF5 oncogenic module governing SRC-induced cancer stemness and metastasis in TNBC. Therefore, targeting YAP1/KLF5-mediated transcription may provide a promising strategy for TNBC treatment with SRC aberrantly activation.
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